**2. Epidemiology**

Approximately 750,000 persons in the United States alone experience an ischemic stroke each year [1]. Stroke care expense for the United States healthcare system was 74 billion dollars

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based on 2010 economic data and with the aging American population and higher incidence of obesity and diabetes in young adults, this cost to the American economy will increase [2]. An interesting analysis was published demonstrating that approximately 120 million neurons (equivalent to 714 kilometers or 444 miles of myelinated fibers) are lost each hour after a large arterial occlusion, thereby accelerating brain aging by 3.6 years per hour of ischemia time [3]. This neuronal loss often translates into permanent and devastating neurological sequelae.

composed of a luminal endothelial layer consisting of an internal elastic lamina and a fibro‐ collagenous tissue layer, the latter two of which are thrombogenic. This tissue layer is covered externally by the tunica media consisting of smooth muscle cells followed by a fibrocollage‐ nous layer composed of the external elastic lamina and an external fibrous serosa layer, which composes the tunica adventitia layer. Carotid stenosis is thought to form as a result of intimal endothelial injury by mechanical hemodynamic shear stresses and metabolic and inflamma‐ tory processes. The plaque material often contains macrophages, inflammatory cells, calcium, lipid and cholesterol deposits, thought to be formed as part of the healing process after

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After disruption of the arterial endothelial lining, expression of inflammatory cell adhesion markers such as VCAM-1, ICAM and other receptors are upregulated [1,7]. Additionally, platelets adhere to the disrupted endothelium after balloon angioplasty and they degranu‐ late, thereby releasing various cytokines and growth factors including transforming growth factor beta (TGF-β), epidermal growth factor (EGF) and platelet derived growth factor (PDGF) [1,8].These resultinmigrationandproliferationofthevascular smoothmuscle cellsofthe tunica mediatoformaneointimallayerinanattempttohealthedisruptedendothelium.Thisneointima becomes more permeable to inflammatory cells as degranulated platelets adhere and remod‐ el the site of the injured intima [1,9,10]. T-cells, monocytes and lipid laden macrophages are seen in these plaques as they become more chronic, and calcium is often deposited during this process in an attempt to stabilize the plaque. Plaques with less calcification tend to be more vulnerable to rupture or thrombosis, indicating that the deposition of calcium appears to be protective and helps to stabilize the plaque by encasing the inflammatory materials,ratherthan

leaving them exposed for further exacerbation of the inflammatory process [1,11].

and the lumen becomes progressively more narrowed [1].

plaque volume and presence and location of a necrotic core [12].

**5. Presentation and radiographic evaluation**

The proliferation of smooth muscle cells is accompanied by an increase in matrix metallopro‐ teinases (MMPs) such as MMP-2 and MMP-9, which help to remodel the vessel by dilating the stenotic segment, thereby initially compensating for the loss of intimal diameter by the early plaque. However, with progression of the plaque thickness, the vessel eventually can no longer dilate further to compensate once the plaque occupies about 40-50% of the luminal diameter,

Vascular stenosis alone does not appear to correlate well with predicting which asymptomatic plaques will result in cerebrovascular symptoms, and therefore additional information about the plaque characteristics are important to assess the vulnerability of the plaque to progress and become symptomatic. Factors which appear to be important in identifying vulnerable plaques include echolucency of the plaque on high resolution B-mode ultrasound, absence of calcification, presence of intraplaque hemorrhage, surface irregularity, fibrous cap thickness,

The history alone can often give a great clue to the underlying cause of the carotid stenosis, once identified. Atherosclerotic disease is the most common cause of carotid stenosis, and is

endothelial injury [1].

It has been estimated that 20-30% of ischemic strokes result from extracranial carotid artery stenosis secondary to atherosclerotic disease [4,5]. Atherosclerosis is a chronic progressive process associated with modifiable risk factors that promote chronic inflammatory events within the arterial wall. Progression of atherosclerotic plaque formation causes ischemic stroke generally by one of two mechanisms: either a flow-limiting stenosis of the arterial lumen resulting in cerebral hypoperfusion typically in the watershed territories or more commonly, thromboembolic events from ruptured atherosclerotic plaque. Until one of these events causes a stroke, carotid stenosis remains asymptomatic and often goes undetected.

The prevalence of carotid stenosis can vary widely with geographic location due to cultural, genetic, and socioeconomic differences. The acquired nature of atherosclerotic disease implies that several of the risk factors that contribute to its development can be modified by individual changes in lifestyle, diet, and medical management.
